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NURS 2050
Cynthia Barkhouse Mckeen

Antidepressants: Clinical Depression: We already know the DX. This is not being tested  Several theories re: pathogenesis, remains unknown 1. Monoamine theory: ↓ functional amine-dependent synaptic transmission (NE/ 5HT or both) - Simplistic: much more complex than just restoring NT levels  However, most drugs affect synaptic transmission for NE and 5HT by: 1. Metabolism 2. Reuptake 3. Antagonism at receptor 5HT= Serotonin Antidepressants: 1. TCAs- Tricyclic Antidepressants 2. SSRIs - Selective serotonin reuptake inhibitors 3. SNRIs - Serotonin-noradrenaline reuptake inhibitors 4. NDRIs- Noradrenaline – dopamine reuptake inhibitors 5. NaSSA - Noradrenergic and specific serotonergic antidepressant - 6. MAOIs - Monoamine oxidase inhibitors - 7. Reversible inhibitors of MAO-A - RIMAs Add on agents (augmentation): 1. Lithium 2. Atypical antipsychotics 3. Thyroid hormone 4. Folic acid 5. 2 antidepressant Antidepressants: Uses 1. Depression 2. Anxiety disorders 3. Neuropathic pain 4. Migraine 5. Insomnia 6. Premature ejaculation Tricyclic Antidepressants (TCAs)  Uses: depression, anxiety, neuropathic pain, migraine prophylaxis, insomnia  Meds: amitriptyline, imipramine imipramine, doxepin doxepin, clomipramine clomipramine, nortriptyline, desipramine  3‐ringed chemical structure (imipramine‐1950s)  Mechanism of action: – re‐uptake inhibition of NE & 5‐HT (balance varies) Fig. 32-2. Mechanism of action of tricyclic antidepressants. A, Under drug-free conditions, the actions of norepinephrine and serotonin are terminated by active uptake of these transmitters back into the nerve terminals from which they were released. B, By inhibiting the uptake pumps for norepinephrine and serotonin, tricyclic antidepressants (P = uptake pump, T = transmitter [norepinephrine or serotonin], TCA = tricyclic antidepressant, P = uptake pump.) Its NOT selective! It binds to other receptors too! Adverse effects 1. TCAs – can block: 1. Muscarinic Receptors: causing anticholinergic Side Effects: Dry mouth, confusion, blurred vision, urinary retention 2. Histamine Receptors: causing Sedation, weight gain 3. Α‐Adrenergic Receptors: causing orthostatic hypotension 2. Cardiac conduction issues: 1. ↓ vagal influences on the heart (secondary to muscarinic blockade) 2. act on the bundle of HIS to ↓ conduction 3. can block cardiac Na+ and K | + 3. Sexual dysfunction 4. Lower the seizure threshold Points to Note: • “ Toxic” in overdose – Caution in those patients with suicidal ideation (because OD = toxic) – Clinical manifestations (of toxicity) • Cardiotoxicity (QRS prolongation, QT prolongation = rhythm problems) • Agitated delirium • Seizures (decreases the threshold so that you get more seizures) • Effects of peripheral muscarinic blockade (hyperthermia, flushing, dry mouth, dilation of pupils) • Dysrrhythmia: Do not treat with antiarrhythmics that also block sodium channels. Selective serotonin reuptake inhibitors (SSRIs) taper, taper, taper! Never stop drug all at once! Uses: depression, anxiety (various disorders), etc  Chemically heterogeneous, many different agents Method Of Action: specific and selective for inhibiting 5‐HT reuptake • Less histaminic, anticholinergic or alpha blocking side effects Examples: • Citalopram (Celexa) • Fluvoxamine (Luvox) • Escitalopram (Cipralex) • Sertraline (Zoloft) • Fluoxetine (Prozac) • Paroxetine (Paxil) Side Effects: **usually side effect free, relatively safe in monosubstance overdoses 1. GI distress (Nausea 25‐50%) 2. Sexual dysfunction (dose related, 25%) 3. Nervousness, insomnia (except fluvoxamine), anxiety 4. Potent CYP 2D6, 1A2, 3A inhibitor
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